Aristolochic acid-induced accumulation of methylglyoxal and Nε-(carboxymethyl)lysine: An important and novel pathway in the pathogenic mechanism for aristolochic acid nephropathy
Aristolochic acid-induced accumulation of methylglyoxal and Nε-(carboxymethyl)lysine: An important and novel pathway in the pathogenic mechanism for aristolochic acid nephropathy
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DOI：
10.1016/j.bbrc.2012.06.049
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发表时间：
2012-07-13
影响因子：
3.1
通讯作者：
Lee, Jen-Ai
中科院分区：
文献类型：
--
作者：
Li, Yi-Chieh;Tsai, Shin-Han;Lee, Jen-Ai
马兜铃酸，发现在马兜铃属物种，导致马兜铃酸肾病（AAN），并可能发展成肾衰竭。甲基乙二醛（MGO）是葡萄糖或脂肪酸代谢过程中产生的高细胞毒性化合物。它与蛋白质结合并形成N-β-（羧甲基）赖氨酸（CML），这有助于衰老和糖尿病并发症。然而，没有相关文献探讨MGO和CML与AAN的关系。通过连续5天给C3 H/He小鼠注射AA（10 mg/kg BW），我们成功地建立了AAN模型，并观察到肾小管萎缩伴肾功能下降。肌酐清除率也从10.32 +/- 0.79 ml/min/kg降至2.19 +/- 0.29 ml/min/kg（p <0.05）。
Aristolochic acid, found in the Aristolochia species, causes aristolochic acid nephropathy (AAN) and can develop into renal failure. Methylglyoxal (MGO) is a highly cytotoxic compound generated from the metabolic process of glucose or fatty acids. It binds to proteins and forms N-epsilon-(carboxymethyl)lysine (CML), which contributes to aging and diabetes mellitus complications. However, no relevant literature explores the relationship of MGO and CML with AAN. By injecting AA (10 mg/kg BW) into C3H/He mice for 5 consecutive days, we successfully developed an AAN model and observed tubular atrophy with decreased renal function. Creatinine clearance also decreased from 10.32 +/- 0.79 ml/min/kg to 2.19 +/- 0.29 ml/min/kg (p